Decreased SOD Activity Research Articles

Antioxidant Properties and Protective Effect of Aqueous Anti-Ulcer Drug (AQAUD) against Aspirin-induced Gastric Ulcers in Albino Rats

Aim: The aim of this study is to evaluate the antioxidant properties and protective effects of aqueous anti-ulcer drug (AQAUD) against aspirin-induced gastric ulcer in albino rats.
 Methods: In this study, 30 male albino rats were divided into 5 groups of 6 each. Rats in group I served as normal control and received food and water. Animals in group II received food and water in addition to aspirin (400 mg/kg.b.wt) orally on the 14th day. Rats in groups III, IV and V received “AQAUD” (250 mg/kg.b.wt), (500 mg/kg.b.wt) and Omeprazole (20 mg/kg.b.wt) respectively for 14 days and aspirin (400 mg/kg.b.wt) orally on the 14th day. In vitro antioxidant property of “AQAUD” was assessed by its nitric oxide and hydroxyl radicals scavenging properties. The ulcer protective effect of “AQAUD” was assessed by determining the free and total acidity, ulcer index and % protection in the stomach content. The antioxidant potential in animals was evaluated by determining the concentrations of malondialdehyde and reduced glutathione. Superoxide dismutase and catalase activities were assayed in the stomach homogenates to further assess antioxidant potential. Total phenolics and flavonoid compounds were quantified to know the antioxidant content. Histopathological assessment of the gastric mucosa was used to assess the protective potentials of “AQAUD”. Data were analyzed using Statistical Package for Social Science (SPSS) version 21.
 Results: The results revealed that free acidity and ulcer indexes were significantly (p<0.05) reduced by “AQAUD”. There was a significant decrease in SOD activity of the stomach homogenates when compared to the aspirin group, with values for “AQAUD” 250 mg/kg.b.wt and “AQAUD” 500 mg/kg b.wt as 37.24±5.39ux10-2/mg protein and 23.64±2.91ux10-2/mg protein respectively. Result of acute toxicity testing showed that “AQAUD” is generally safe up to 5000 mg/kg b.wt.
 Conclusion: The results revealed that treatment with aspirin caused loss of gland architecture with erosion of epithelial layer, but AQAUD treatment ameliorated the effect of aspirin administration. The study revealed that “AQAUD” has considerable antioxidant potentials and can effectively protect against gastric ulcers.

Coniferyl ferulate exerts antidepressant effect via inhibiting the activation of NMDAR-CaMKII-MAPKs and mitochondrial apoptotic pathways

Xiaoyaosan (XYS), composed of Radix Bupleuri, Radix Angelicae Sinensis, Radix Paeoniae Alba, Rhizoma Atractylodis Macrocephalae, Poria, Herba Menthae, Rhizoma Zingiberis Recens and Radix Glycyrrhizae, is a valuable traditional Chinese medicine (TCM) which is used for the treatment of depression in China. In our previous experiments, we found that coniferyl ferulate (CF) was the main active constituent of Xiaoyaosan based on UPLC-PDA guided isolation technique. However, the antidepressant effect and mechanisms of CF is still unknown. In the current study, we aim to explore the possible mechanisms involved in the neuroprotective effect of CF in glutamate-injured PC12cells, and further to confirm the anti-depressant effect of CF on the model of behavioral despair in vivo. The model of glutamate-injured PC12cells was employed to investigate the possible mechanisms involved in the neuroprotective effect of CF. The model of behavioral despair was carried out to examine the in vivo anti-depressant effect of CF. The results showed that CF significantly attenuated the decrease of cell viability, the release of lactate dehydrogenase (LDH), and the increase of apoptosis rates induced by glutamate. CF could also suppress the influx of Ca2+ and the elevation of p-NR2B, p-CaMK II, p-JNK, and p-p38 level induced by glutamate. Besides, CF could also inhibit the generation of reactive oxygen species (ROS), the decrease of SOD activity, the elevation of malondialdehyde (MDA) level, and suppress the loss of mitochondrial membrane potential (MMPs) and the activation Bcl-2/Bax mediated apoptotic pathways induced by glutamate. Furthermore, CF obviously decreased the immobility time in tail suspension test (TST) and forced swimming test (FST). In conclusion, CF exert the indeed anti-depressant effect. The inhibition of NMDAR-CaMKII-MAPKs signaling pathway, oxidative stress, and mitochondrial apoptotic pathways were involved in the anti-depressant effect of CF.

ВОССТАНОВЛЕНИЕ РАСТЕНИЙ ТАБАКА ПОСЛЕ ОБРАБОТКИ ИОНАМИ МЕДИ

The aftereffects of copper ions (100 and 300 μM) on the organ size, the content of stress markers (hydro-gen peroxide, lipid peroxidation - LPO) and components of the antioxidant status (superoxide dismutase - SOD and guaiacol peroxidase - GPO) were studied in the roots, stem, and leaves of Nicotiana tabacum L. It was shown that tobacco plants were sensitive to long-term exposure to 100 and 300 μM Cu2+. Both concentrations inhibited root growth, while shoot length and thickness, and leaf area decreased only in the case of pretreatment with 300 μM Cu2+. So, the growth of aboveground organs was suppressed signifi-cantly less than the root. The level of lipid peroxidation and the content of hydrogen peroxide in the roots under these conditions were also higher, which indicates a stronger stress, compared to stem and leaf. The activity of antioxidant enzymes SOD and GPO in roots and aboveground organs specifically changed de-pending on the concentration of copper ions and the type of organ. In the roots, there was a decrease in SOD activity and an increase in the activity of GPO under pretreatment with 300 μM Cu2+, compared to the control and 100 μM Cu2+, while in stem and leaves the activity of enzymes decreased. The data ob-tained indicate incomplete plant recovery under the aftereffect of copper ions.

Effects of intragastric administration of La2O3 nanoparticles on mouse testes.

Lanthanum oxide (La2O3) nanoparticles (NPs) have been widely used in photoelectric and catalytic applications. However, their exposure and reproductive toxicity is unknown. In this study, the effect of the intragastric administration of two different-sized La2O3 particles in the testes of mice for 60 days was investigated. Although the body weight of mice treated or not treated with La2O3 NPs was not different and La2O3 NPs were distributed in the organs including the testis, liver, kidney, spleen, heart and brain. La2O3 NPs accumulate more than micro-sized La2O3 (MPs) in mice testes. The histopathological evaluation showed that moderate reproductive toxicity induced by La2O3 NPs in the testicle tissues. Furthermore, increased MDA, 8-OHdG levels and decreased SOD activities were detected in the La2O3 NP-treated groups. Moreover, qRT-PCR and western blotting data indicated that La2O3 NPs affecting the blood-testis barrier (BTB)-related genes in mice testes. Taken together, these findings suggested that La2O3 NPs activated inflammation responses and cross the BTB in the murine testes. This study provided useful information for risk analysis and regulation of La2O3 NPs by administrative agencies.

Differential Tolerance and Phenolic Leaf Profile in Response to Boron Supply in Two Highbush Blueberry Genotypes

Highbush blueberry (Vaccinium corymbosum L.) is beneficial for human health due to its bioactive properties. Agronomic management includes boron (B) addition to promote its growth and development. We aimed to provide new insights into the effects of B supply on the phenolic profile and antioxidative capacity in the leaves of two common cultivars, Brigitta and Legacy. Seedlings of Brigitta and Legacy were supplied with different B concentrations (0–50 mg B L−1). After 30 days, leaf biomass and B content, the activity of phenylalanine-ammonia-lyase (PAL, EC 4.3.1.24), the phenolic profile, and radical scavenging activity of methanolic extracts (oxygen radical absorbance capacity (ORAC), reducing 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ferric reducing-antioxidant power (FRAP)) were analyzed. Tolerance to B was assessed by the lipid peroxidation level and superoxide dismutase (SOD, EC 1.15.1.1) activity. Leaf biomass in cultivars increased at 3 mg B L−1, while Legacy was more sensitive to higher B treatments than Brigitta, which was evidenced by increased lipid peroxidation and decreased SOD activity. Boron-induced inhibition of PAL activity was higher in Legacy. Cultivar-specific differences observed in hydroxycinnamic, flavonoid, and anthocyanin profiles of leaf extracts were related to radical scavenging capacities. The results indicate different B requirements in the two blueberry genotypes, which should be considered before B application to obtain an optimal antioxidant composition. Boron supply increased the accumulation of flavonoids in Brigitta and hydroxycinnamates in Legacy. Higher tolerance to excess B in Brigitta may be related to higher antioxidative capacity and SOD activity than Legacy.

Oxidative Stress Induced DNA Damage and Reproductive Toxicity in Male Albino Mice Orally Exposed to Sorbitol

Abstract In this study, the potential DNA damage and reproductive toxicity of sorbitol was investigated using bone marrow micronucleus (MN), sperm morphology, and sperm count in mice. Five doses of 90, 45, 20, 10 and 1 mg/kg/day, defined by allometry, and approximately corresponding to 1.5g, 750mg, 330mg, 165mg and 16mg of sorbitol daily consumption by a 70kg human, respectively, were used. MN analysis showed a dose-dependent induction of micronucleated polychromatic erythrocytes and other nuclear abnormalities across the treatment groups. Assessment of sperm shape showed a significant (p < 0.05) increase in sperm abnormalities with significant (p < 0.05) decrease in mean sperm count in treated groups. The result of the oxidative stress biomarkers showed induction of significant (p < 0.05) increase in liver catalase, MDA and serum ALT and AST activities with concomitant decrease in SOD activities in exposed mice. A significant increase in weight of exposed mice were recorded when compared with the negative control. The results of this study showed the genotoxicity and reproductive effects of sorbitol.

Evaluation of reproductive and renal toxicity of varenicline in male rats.

Objective(s):Varenicline is a selective partial agonist for the nicotinic acetylcholine receptor a4b2 subtype, which is widely used to treat smoking addiction. However, there is still no data about its potential toxic effects on tissues. In this study, we aimed to determine the varenicline-induced toxicity on reproductive and renal tissues in rats.Materials and Methods:Rats were randomly divided into two groups: control (n=10) and varenicline (n=24). Then, rats in each group were sub-divided equally as acute and chronic groups. The control rats were orally given distilled water only. Varenicline was administrated orally as follows: 1st–3rd days 9 µg/kg/day, 4th–7th days 9 µg/kg twice daily, and 8th–90th days 18 µg/kg twice daily. The rats of acute and chronic groups were sacrificed on the 45th and 90th days, respectively. Some tissue markers related to oxidative stress were measured, and sperm characteristics were observed.Results:In the acute group, varenicline led to a significant decrease in SOD activities in both kidney and testis tissues. In the chronic group, varenicline significantly increased MDA and MPO production, and reduced CAT and GPx levels in the kidneys and testes. Also, SOD and GSH levels significantly decreased in the testes. Moreover, sperm characteristics were negatively affected; histopathological deformation was observed in the testes and kidneys in all groups.Conclusion:This study showed that varenicline could detrimentally affect the kidneys and testes in both acute and chronic term usage. Further studies will provide more insights into the molecular dynamics of this damage.

Regulation of Lnc-NTF3-5 on islet β-cell dysfunction in high glucose environment and related mechanisms.

The pathogenesis of diabetes is closely related to islet β-cell dysfunction. Lnc-NTF3-5 participates in the occurrence and development of various diseases. However, Lnc-NTF3-54's effect on islet β-cell dysfunction in high glucose environment remains unclear. The islet β cell MIN6 cells were cultured in vitro and randomly divided into control group, high glucose group, NTF3-5 siRNA group, and NTF3-5 group, which was respectively transfected with Lnc-NTF3-5 siRNA and Lnc-NTF3-5 plasmid under high glucose condition. Lnc-NTF3-5 expression was measured by real time PCR and cell proliferation was assessed by MTT assay. In addition, Caspase 3 activity, SOD activity, and ROS content were also detected along with the secretion of IL-10 and IL-1 by enzyme-linked immunosorbent assay (ELISA). Compared with control group, Lnc-NTF3-5 expression in MIN6 cells was significantly increased in high glucose environment (p<0.05). In high glucose environment, Lnc-NTF3-5 plasmid transfection up-regulated Lnc-NTF3-5 expression, inhibited cell proliferation, increased Caspase 3 activity, and decreased SOD activity. Meanwhile, Lnc-NTF3-5 plasmid also increased ROS content and IL-1 level, and decreased IL-10 level and insulin secretion. Compared with high glucose group, the differences were statistically significant (p<0.05). However, transfection of Lnc-NTF3-5 siRNA down-regulated Lnc-NTF3-5 expression under high glucose environment and reversed the above changes. Compared with high glucose group, the differences were statistically significant (p<0.05). Lnc-NTF3-5 expression is increased in high glucose environment. Targeting Lnc-NTF3-5 can inhibit islet cell apoptosis, oxidative stress, and promote islet cell proliferation and insulin secretion.

Rosuvastatin Calcium Affects Alzheimer's Disease Through Regulating Defensive Transduction Pathways of Oxidative and Chemical Stress Signaling Pathway

Alzheimer's disease (AD) treatment is not effective. Statins are lipid-lowering drugs. However, the role and mechanism of statins for treating AD remains unclear. SD rats were separated into sham operation group; AD group and rosuvastatin calcium group followed by analysis of cognitive function and neuronal morphology. ELISA was to measure the level of TNF-α and IL-1; SOD activity and ROS levels were measured,. Real-time quantitative PCR was to analyze Bcl-2 and Bax level. The expression of Nuclear Erythroid 2-Related Factor 2/Antioxidant Responsive Element (NRF2/ARE) signaling pathway was analyzed by Western blot. Compared with sham operation group, the cognitive ability of the AD group was significantly decreased; with elevated secretion of TNF-α and IL-1, decreased SOD activity, increased ROS generation, decreased Bcl-2 expression as well as increased Bax expression (P &lt; 0.05). In addition, AD group rats showed neuronal damage in the hippocampus and decreased expression of NRF2 and ARE. However, rosuvastatin calcium treatment improved cognitive ability, decreased TNF-α and IL-1 secretion, increased SOD activity, decreased ROS content, increased Bcl-2 expression and decreased Bax expression as well as ameliorated neuronal damage, increased number of nerve cells, and increased expression of NRF2 and ARE. Rosuvastatin calcium can inhibit the oxidative stress and inflammation, inhibit the apoptosis of hippocampus cells and improve the cognitive ability of AD rats by regulating NRF2/ARE signaling pathway.

Effect of Long-Chain Non-Coding RNA GAS5 on Osteogenic/Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Under Oxidative Stress Through Targeting MiR-365

Oxidative stress affects BMSCs. LncRNA GAS5 regulates cell proliferation and apoptosis. However, the effect of LncRNA GAS5 on osteogenesis/adipogenic differentiation of BMSCs under oxidative stress has not been reported. Rat BMSCs were cultured and randomly divided into 4 groups, normal control group; oxidative stress group; GAS5 siRNA group; GAS5 siRNA+ miR-365 inhibitor group followed by analysis of LncRNA GAS5 expression by Real time PCR, cell proliferation by MTT assay, Caspase3 activity, GAS5 and miR-365 targeting relationship by luciferase reporter assay, ALP activity, expression of Runx2, OP and PPAR 2 by Real time PCR, as well as ROS content and SOD activity. In oxidative stress group, GAS5 expression was significantly increased along with inhibited cell proliferation, increased Caspase3 activity, decreased ALP activity and the expression of Runx2 and OP, increased PPAR 2 expression and ROS content, and decreased SOD activity compared to control group (P &lt; 0 05). miR-365 was the target miRNA of GAS5. GAS5 siRNA down-regulated GAS5 expression, significantly promoted cell proliferation, inhibited Caspase3 activity, increased ALP activity and Runx2 and OP expression, decreased PPAR 2 expression and ROS content, and increased SOD activity. (P &lt; 0 05). However, GAS5 siRNA+ miR-365 inhibitor group reversed the effect of GAS5 siRNA. Oxidative stress promotes LncRNA GAS5 expression in BMSCs. LncRNA GAS5 regulates oxidative stress by targeting miR-365. Knockdown of GAS5 can promote BMSCs proliferation and osteogenic differentiation and inhibit adipogenic differentiation under oxidative stress.

Effect of Mir-663 on the Differentiation of Bone Marrow Mesenchymal Stem Cells in Inflammatory Environment Through Regulating Oxidative Stress and Transforming Growth Factor β1

BMSCs are beneficial for the treatment of Osteoarthritis (OA). Mir-663 involves in various diseases. However, the role of Mir-663 in the differentiation of BMSCs in an inflammatory environment remains unclear. Rat BMSCs were isolated and divided into control group, and inflammation group which was treated with 1 μg/ml lipopolysaccharide (LPS), Mir-663 group and Mir-663 siRNA groups which was respectively transfected with Mir-663 plasmid and Mir-663 siRNA into LPS-treated BMSCs followed by analysis of the survival rate of BMSC by MTT, Caspase 3 activity, ALP activity, expression of osteogenic genes Runx2 and OP by Real time PCR, ROS content and SOD activity, TGF-β1 level by Real time PCR and ELISA, TNF- and IL-1 secretion by ELISA. LPS treatment significantly increased Mir-663 expression, inhibited cell proliferation, increased Caspase 3 activity, and inhibited ALP activity. Meanwhile it also significantly decreased Runx2 and OP expression, increased ROS content, decreased SOD activity and TGF-β1 expression as well as elevated TNF-α and IL-1β secretion compared to control (P &lt; 0.05); Mir-663 plasmid transfection can further promote the above changes (P &lt; 0.05); whereas, Mir-663 siRNA could reverse the above changes (P &lt; 0.05). Mir-663 expression was increased in BMSCs in inflammatory environment. Down-regulation of Mir663 expression can regulate oxidative stress, up-regulate TGF-β1 level, inhibit the secretion of TNF-α and IL-1β, and promote the proliferation and osteogenic differentiation of BMSCs in inflammatory environment.

Role of mitochondrial DNA in oxidative damage induced by sodium arsenite in human bronchial epithelial cells

ABSTRACTLong-term exposure to sodium arsenite was found to induce malignant transformation in human bronchial epithelial (HBE) cell line as evidenced by elevated ROS levels. Although chronic sodium arsenite-induced HBE cell line transformation was associated with elevated ROS generation, it was of interest to determine whether acute sodium arsenite exposure also initiated pulmonary damage. Thus, the aim of this study was to investigate oxidative-stress-related pulmonary damage using a human bronchial epithelial (HBE) cell line. Incubation of ρ+-HBE (in the presence of mitochondrial DNA) cells with various concentrations of sodium arsenite, significantly increased ROS and MDA levels accompanied by decreased SOD activity in a concentration-dependent manner. In contrast, treatment of ρ–HBE (without mitochondrial DNA) cells various concentrations of sodium arsenite a reduction in ROS and MDA levels were noted. However, the SOD activity remained decreased in ρ–HBE cells. This was accompanied by a significant rise in HO-1 protein expressions levels in both cell types with greater changes ρ–HBE cells at the lower sodium arsenite concentrations. Data indicate that acute sodium arsenite exposure exerted a greater effect ρ–HBE cells suggesting that absence of mitochondrial DNA appears to enhance sensitivity to the oxidant actions of inorganic As.

Osteoprotegerin Protects H2O2-Induced Bone Marrow Mesenchymal Stem Cells Damage

Oxidative stress causes damage and apoptosis of bone marrow mesenchymal stem cells (BMSCs). Osteoprotegerin (OPG) regulates bone differentiation. However, whether OPG plays a role in osteogenic/adipogenic differentiation under oxidative stress remains poorly understood. Rat BMSCs were randomly divided into control group; H2O2 group, in which H2O2 was used to prepare oxidative stress model; OPG group, in which 5 μM OPG was added to BMSCs based on oxidative stress model followed by analysis of BMSCs proliferation by MTT assay, BMSCs apoptosis, expression of RUNX2, OPN, FABP4 and PPARγ2 by real time PCR, OPG and RANKL protein expression by Western blot as well as SOD activity and ROS content by spectrophotometry. Compared with control group, H2O2 significantly decreased BMSCs proliferation, increased Caspase 3 activity, downregulated RUNX2 and OPN, upregulated FABP4 and PPARγ2, decreased SOD activity and increased ROS content (P &lt; 0.05). Under H2O2 treatment, OPG addition significantly promoted BMSCs proliferation, decreased Caspase 3 activity, increased RUNX2 and OPN expression, decreased FABP4 and PPARγ2 expression, increased SOD activity, and decreased ROS content and RANKL expression (P &lt; 0.05). OPG can promote osteogenic differentiation of BMSCs under oxidative stress, inhibit adipogenic differentiation, and protect BMSCs from damage and promote BMSCs proliferation by regulating OPG/RANKL signaling pathway.

4,4′-Dichlorodiphenyl diselenide reverses a depressive-like phenotype, modulates prefrontal cortical oxidative stress and dysregulated glutamatergic neurotransmission induced by subchronic dexamethasone exposure to mice

Dexamethasone (DEX) is a synthetic agonist of glucocorticoid receptors that has been associated with neurotoxicity and neuropsychiatric diseases. (p-ClPhSe)2 is an organoselenium compound reported to have antioxidant, antidepressant-like, and neuroprotective actions. This study investigated whether antioxidant activity and modulation of the glutamatergic system contribute to the antidepressant-like effect of (p-ClPhSe)2 in mice subchronically exposed to DEX. Swiss mice received intraperitoneal injections of DEX (2 mg/kg) or saline (vehicle) once a day for 21 days. After, the mice received (p-ClPhSe)2 (1–10 mg/kg) or mineral oil (vehicle) by the intragastric route (i.g.) for 7 days. The mice exposed to DEX were treated with fluoxetine (20 mg/kg, i.g.) once a day for 7 days. 24 h after the last treatment, the animals performed the locomotor activity (LMA), tail suspension, and forced swimming tests. Ex vivo assays were performed in samples of prefrontal cortex (PFC). The results show that (p-ClPhSe)2 reversed depressive-like behavioral phenotype induced by DEX without affecting LMA. Further, (p-ClPhSe)2 at all doses reduced ROS levels and increased CAT activity in the PFC of DEX-exposed mice. The highest dose of (p-ClPhSe)2 was effective against the decrease of SOD activity in the PFC of mice exposed to DEX. (p-ClPhSe)2 increased the [3H] glutamate uptake/release and decreased the Na+/K+-ATPase activity as well as the EAAT1 and NMDA R2A protein contents in the PFC of DEX-exposed mice. Regarding the NMDA R2B levels, there was no difference among experimental groups. In conclusion, this study reveals the effectiveness of (p-ClPhSe)2 in reversing the depressive-like phenotype of DEX-exposed mice. In addition, (p-ClPhSe)2 modulated oxidative stress and glutamate neurotransmission in the PFC of mice subchronically exposed to DEX.

Sickling-preventive effects of rutin is associated with modulation of deoxygenated haemoglobin, 2,3-bisphosphoglycerate mutase, redox status and alteration of functional chemistry in sickle erythrocytes

Sickle cell anaemia is a hereditary disease branded by an upsurge in generation of ROS, irregular iron release and little or no antioxidant activity which can lead to cellular injuries due to oxidative stress resulting in severe symptoms including anaemia and pain. The disease is caused by a mutated version of the gene that helps make haemoglobin, the protein that carries oxygen in red blood cells. We used in silico and in vitro experiments to examine the antisickling effects of rutin for the first time by means of before and after induction approaches in sickle erythrocytes. Rutin was docked against deoxy-haemoglobin and 2,3-bisphosphoglycerate mutase, revealing binding energies (-27.329 and -25.614 kcal/mol) and Ki of 0.989μM and 0.990 μM at their catalytic sites through strong hydrophobic and hydrogen bond interactions. Sickling was thereafter, induced at 3 h with 2% metabisulphite. Rutin prevented sickling maximally at 12.3μM and reversed same at 16.4μM, by 78.5% and 69.9%, one-to-one. Treatment with rutin significantly (P < 0.05) reinvented the integrity of erythrocytes membrane as evident from the practical % haemolysis compared to induced erythrocytes. Rutin also significantly (P < 0.05) prevented and reversed lipid peroxidation relative to untreated. Likewise, GSH, CAT levels were observed to significantly (P < 0.05) increase with concomitant significant (P < 0.05) decrease in SOD activity based on administration of rutin after sickling induction approach. Furthermore, FTIR results showed that treatment with rutin favourably altered the functional chemistry, umpiring from shifts and functional groups observed. It can thus be deduced that, antisickling effects of rutin may be associated with modulation of deoxy-haemoglobin, 2,3-bisphosphoglycerate mutase, alteration of redox homeostasis and functional chemistry of sickle erythrocytes.

Silver nanoparticles testicular toxicity in rat

To evaluate the potential testicular toxicity induced by silver nanoparticles (AgNPs) in Sprague Dawley rate. The protocol study was designed as follows: G1: 30 adult male rats were kept as control. G2: 30 adult male rats were administered 5.36 mg/kg of AgNPs orally, twice weekly for six months. G3: 30 adult male rats were administered 13.4 mg/kg of AgNPs orally, twice weekly for six months. The results of hormonal assay revealed that a significant decrease in testosterone level while a significant increase in LH level was obtained. The testicular homogenate showed a significant decrease in SOD activity accompanied by a significant increase in MDA level in both G2 and G3 in comparison with the control in a dose-response relationship. Sperm viability indicates a significant decrease in rats in G2 and G3 groups. A significant decrease in DNA chromatin integrity % was obtained in rats of G3 in comparison with G2 and control. The semithin and TEM sections of the testis of G2 and G3 groups showed Sertoli cells have vacuolations with a disturbance in the arrangement and the staining affinity of spermatogenic cells. The spermatogonia appeared with a moderate electron density of the nucleus and cytoplasm. The acrosome and its cap become oval and light electron dens of spermatid cells.

Nitric Oxide-Mediated Modulation of Functional Iron Status in Iron-Deficient Maize Plants

Nitric oxide is reported to alleviate Fe-deficiency effects, possibly by enhancing the functional Fe status of plants. Study describes changes in leaf tissue Fe status and consequent modulation of oxidative stress and antioxidant defense in Fe-deficient maize (Zea mays L.) plants supplied with NO. Supply of sodium nitroprusside (SNP), but not of sodium ferrocyanide (SF), caused regreening of leaves, syntheses of chlorophylls and carotenoids and increased activities of hydrogen peroxide-scavenging heme-Fe enzymes and lipid peroxidation, decreased SOD activity and hydrogen peroxide concentration. Though SNP or SF appears to donate Fe and increase leaf active Fe, the later did not induce increases in chlorophyll and carotenoids, and therefore NO appears to have a role in Fe nutrition irrespective of total or active Fe status of plants.

SOD activity in the end stage knee and hip osteoarthritic cartilage significantly lower than non osteoarthritic cartilage independent of age-related change

Purpose: Recent study has shown that SOD gene expression level or protein level does not necessarily reflect SOD activity since SOD is post-translationally modified after protein synthesis. The trend of SOD activity in end-stage osteoarthritic (OA) tissues remains unknown. The purpose of this study was to examine the possibility of using SOD as an OA biomarker by examining the SOD activity in OA-affected knee cartilage and synovium from patients with end-stage knee OA and in OA-affected femoral head cartilage from patients with end-stage hip OA. Methods: To evaluate the SOD activity in end-stage knee OA cartilage and synovium, samples of cartilage and synovium were taken from the outside of the patellofemoral joint with biopsy forceps. Cartilage and synovium obtained from the knee joint of patients who underwent total knee arthroplasty for end-stage knee OA were defined as end-stage knee OA cartilage and synovium. Cartilage and synovium obtained from the knee joint of patients who underwent knee arthroscopy for meniscal tears or anterior cruciate ligament reconstruction were defined as control specimens. The degree of OA was evaluated using the Kellgren-Lawrence classification. The SOD activity in the samples was analyzed using SOD activity assay based on the auto-oxidation rate of hematoxylin (NWLSS SOD assay). Next, to evaluate the SOD activity in end-stage hip OA cartilage, OA cartilage samples were obtained from the femoral head of patients who underwent total hip arthroplasty for hip OA. Non-OA cartilage samples were obtained from the femoral head of patients who underwent bipolar hip arthroplasty for femoral head neck fractures. The SOD activity in the samples was evaluated using SOD assay based on inhibition of nitroblue tetrazolium reduction (Cayman’s SOD assay). The results of SOD assays are expressed in units per mg protein. This study protocol was approved by the ethics committee of Juntendo Tokyo Koto Geriatric Medical Center. Informed consent was obtained from all patients prior to the study. Results: The SOD activity in end-stage knee OA cartilage was significantly lower than non-OA cartilage (Fig 1A). Furthermore, the SOD activity in end-stage knee OA synovium was significantly lower than that non-OA synovium (Fig 1B). The mean age of the knee OA patients was significantly higher than that of the non-OA patients (Table 1). There was no significant correlation between the SOD activity in the synovium and age (Fig 1D). However, the SOD activity in the cartilage showed a weak negative correlation with age (Fig 1C). Therefore, we cannot deny the possibility that aging induced a decrease in the SOD activity level in the cartilage and synovium of patients with end-stage OA. To investigate the correlation between SOD activity and aging, we focused on the femoral head cartilage, for which it is easy to eliminate the effects of aging. We aimed to prove the causal relationship of SOD activity with aging by comparing the SOD activity in the femoral head cartilage of patients without OA who had a femoral neck fracture and the SOD activity in the femoral head cartilage of patients with hip OA. The average age of non-OA patients with femoral neck fractures was significantly higher than that of patients with end-stage hip OA (Table 2). However, the SOD activity in the femoral head cartilage of patients with hip OA was significantly lower than that of non-OA patients (Fig 2A).There was no significant correlation between the SOD activity in the cartilage and age (Fig 2B). Finally, we evaluated the correlation between NWLSS SOD assay and Cayman’s SOD assay using femoral head cartilage. We found a strong positive correlation between NWLSS SOD assay and Cayman’s SOD assay (Fig 3). Conclusions: It is known that SOD decreases with age. Since SOD activity decreased in knee OA and hip OA cartilage regardless of the age of the control group, it was revealed that the decrease in SOD activity is more related to OA than to age. These data suggested that SOD activity plays an important role in human OA.Table 1Baseline characteristics of patients from Fig 1CharacteristicsControls (N= 10)Knee OA (N =18)P valueAge (years)30.4±14.176.8±9.1< 0.001Gender (Male/female)Male 5, Female 5Male 0, Female 18- Open table in a new tab Table 2Baseline characteristics of patients from Fig 2Characteristicsnon OA (N = 14)hip OA (N = 10)P valueAge (years)82.64±6.4270.0±8.17< 0.001Gender (Male/female)Male 3, Female 11Male 0, Female 11- Open table in a new tab View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Chronic exposure to dichloroacetamide induces biochemical and histopathological changes in the gills of zebrafish.

To evaluate the impact of DCAcAm on zebrafish gill, we measure the responses of antioxidant enzyme (superoxide dismutase, SOD), lipid peroxidation (malondialdehyde, MDA), ATPase (Na+ /K+ -ATPase and Ca2+ /Mg2+ -ATP) and histopathological changes of gill in adult zebrafish, after exposed to different concentrations of DCAcAm (0, 1, 10, 100, and 1000 μg L-1 ) for 30 days. Results indicated that DCAcAm first increased and then decreased SOD activity, and DCAcAm also lowered the activities of Na+ /K+ -ATPase and Ca2+ /Mg2+ -ATPase. These results indicated that high affinity of DCAcAm probably be a main factor, which can damage the structures of enzymes, thereby inhibiting the SOD and ATPase activities. Besides, histopathological investigation results also manifested that chronic exposure to DCAcAm can damage the gill tissues, disrupting the normal function of gills. We conclude that chronic exposure to DCAcAm was harmful to organisms, not only influence gill function, but also further cause damage on the gill tissues.

Comparison and Evaluation of Four Species of Macro-Algaes as Dietary Ingredients in Litopenaeus vannamei Under Normal Rearing and WSSV Challenge Conditions: Effect on Growth, Immune Response, and Intestinal Microbiota.

The study was conducted to compare and evaluate effects of four different macro-algaes on growth, immune response, and intestinal microbiota of Litopenaeus vannamei. In the rearing trial 1, shrimp were fed five diets containing four sources of macro-algaes for 8 weeks, named D1 (without macro-algae), D2 (Porphyra haitanensis), D3 (Undaria pinnatifida), D4 (Saccharina japonica), and D5 (Gracilaria lemaneiformis), respectively. Growth performance of shrimp in D5 diet was significantly higher than that of shrimp fed the control and D4 diet (P < 0.05); however, there is no significant difference among D2, D3, and D5 diets (P > 0.05). Apparent digestibility coefficients of dry matter from the D2, D3, and D5 diets were significantly higher than that from the control and D4 diets (P < 0.05). Supplementary macro-algaes enhanced hepatopancreas immunity through positively increasing total antioxidant status (TAS) and prophenoloxidase activity (ProPO), as well as up-regulating the hepatopancreas RNA expression of ProPO and IκBα and down-regulating the expression of transforming growth factor β. Furthermore, dietary macro-algaes modified intestinal microbiota of L. vannamei, boosting the relative abundance of beneficial bacterial such as Bacteroidetes, Firmicutes, and Bacillaceae, and decreasing those detrimental bacterial such as Gammaproteobacteria and Vibrionaceae. In the white spot syndrome virus (WSSV) challenge trial, shrimps were injected for 6-day after the rearing trial. On the fourth day, shrimp death started to occur, and the mortality in D2, D3, and D5 diets was significantly lower than that in control and SJ diets during 4–6 challenged days (P < 0.05). Dietary macro-algaes ameliorated hepatopancreas damage in L. vannamei by increasing TAS and ProPO activities and decreasing SOD activity, inhibiting the lipid peroxidation (malondialdehyde), as well as regulating the immune-related genes expression. Taken together, dietary macro-algaes availably relieved enterohepatic oxidative damage by improving antioxidant ability and immunity and regulated intestinal microbiota in L. vannamei. These results indicated that G. lemaneiformis is the most suitable macro-algae and then followed by U. pinnatifida and P. haitanensis as the feed ingredient for L. vannamei.